Carbon monoxide (CO) has long been recognized as an environmental hazard and standards for acute exposure have been established. Little attention has been focused, however, upon the effects that chronic exposures to this gas might have although such exposure is relatively common. Cigarette smoking is the major source of carboxyhemoglobin (HbCO) and smokers on the average maintin HbCO levels of 5%. The fetus of a smoking mother caries similar burdens of CO in blood. The proposed research is designed to assess the effects of chronic prenatal CO exposures on the development of the neonatal organism, to determine the permanence of such changes through longitudinal studies, and to determine threshold values below which such effects do not occur. The principal levels of analysis include spontaneous behavioral assessments as well as responses to centrally acting drugs, brain and organ development through protein and DNA analyses, and neurochemical studies designed to measure perturbations in monoamine systems resulting from prenatal hypoxia.